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Abstract
A high concentration (50 μg/ml) of gamma-linolenic acid (GLA) induced morphological
lesions typical of apoptosis, as well as DNA fragmentation, in HeLa cells. A lower
concentration of GLA (20 μg/ml), caused an increased proliferating cell nuclear antigen
(PCNA) labelling, with 92.7% cells positive, compared to 27.7% at a concentration
of 50 μg/ml GLA. In correlation with these results, the number of cells with degraded
DNA below the
peak increased significantly in the 50 μg/ml GLA-treated cells, but increased only
slightly in cells exposed to the lower level of GLA. The high levels of PCNA induced
by 20 μg/ml GLA, in both G1 and S phases, may indicate a state of DNA repair synthesis, whilst at the higher
concentration of GLA, most of the cells became apoptotic. Since apoptosis is associated
with the deregulation of c-Myc expression, and as the Raf-1-MAP kinase cascade activates
the expression of c-Myc and c-Jun, we investigated the effects of 20 and 50 μg/ml
GLA on the Raf-1, c-Myc and c-Jun levels, and on the activity of MAP kinase. The results
showed that 50 μg/ml GLA lowered the activity of MAP kinase. As expected with the
decreased MAP kinase activity in the cells exposed to the higher level GLA, the c-Jun
levels were also lowered. The levels of c-Myc, however, were increased. It is therefore
possible that the deregulated expression of c-Myc in the HeLa cells exposed to the
high level of GLA (50 μg/ml) may contribute to the induction of apoptosis in HeLa
cells.

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Article info
Publication history
Accepted:
May 16,
1996
Received:
February 2,
1996
Identification
Copyright
© 1996 Published by Elsevier Inc.